The Regulation of a Cell’s Ca2+ Signaling Toolkit: The Ca2+ Homeostasome
Abstract
The Ca(2+) ion serves as a ubiquitous second messenger in eukaryotic cells and changes in the intracellular Ca(2+) concentration regulate many responses within a cell, but also communication between cells. In order to make use of such an apparently simple signal, i.e. a change in the intracellular Ca(2+) concentration, cells are equipped with sophisticated machinery to precisely regulate the shape (amplitude, duration) of Ca(2+) signals in a localization-specific manner. To ascertain such a precise regulation, cells rely on the components of the Ca(2+) signaling toolkit. This embraces Ca(2+) entry systems including Ca(2+) channels in the plasma membrane and organellar membranes, and Ca(2+) extrusion/uptake systems including Ca(2+)-ATPases (Ca(2+) pumps) and Na(+)/Ca(2+) exchangers. Besides mitochondria, organelles implicated also in Ca(2+) signaling, cytosolic Ca(2+) buffers are cell-specific subtle modulators of Ca(2+) signals. The Ca(2+)-signaling components not only orchestrate their activity as to ascertain the high accuracy of intracellular Ca(2+) signaling, but they are also implicated in the regulation of their own expression. The total of the molecules that build the network of Ca(2+) signaling components, and that are involved in their own regulation as to maintain physiological Ca(2+) homeostasis resulting in phenotypic stability is named the Ca(2+) homeostasome. Mechanistic details on the functioning of the Ca(2+) homeostasome are presented.
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The observed decrease in PV expression in Shank mutant mice might be viewed as an adaptive or compensatory mechanism to possibly restore (increase) synaptic output according to the concept of the Ca2+ homeostasome.
“In summary, the observed decrease in PV expression in Shank mutant mice might be viewed as an adaptive or compensatory mechanism to possibly restore (increase) synaptic output according to the concept of the Ca2+ homeostasome [104].”
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- Authors
- Schwaller, B.
- Affiliations
- University of Fribourg (CH)
- Corresponding author
- Schwaller, Beat
- ORCID
- Schwaller, Beat
- Venue
- Advances in Experimental Medicine and Biology
- Publisher
- Springer Netherlands
- Published
- 2012
- Volume
- 740
- Pages
- 1-25
- ISSN
- 0065-2598 (ISSN-L)
- OpenAlex
- W104189985
- Cited by
- 54
- References
- 94
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 1 · 2023: 1 · 2022: 2 · 2021: 2 · 2020: 8 · 2019: 6 · 2018: 3 · 2017: 6 · 2016: 2 · 2015: 7 · 2014: 7 · 2013: 4 · 2012: 1
- FWCI
- 11.68
- Type
- book chapter
- Language
- en
- Open access
- closed
- Licence
- Locations
- Advances in experimental medicine and biology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Sensory Systems › Ion Channels and Receptors
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Physiology › Calcium signaling and nucleotide metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion channel regulation and function
- Keywords
- intracellular calcium signaling, calcium homeostasis, calcium channels, calcium pump, Na+/Ca2+ exchanger, mitochondria, second messengers
- MeSH terms
- Animals, Calcium, Cell Membrane, Cytosol, Homeostasis, Humans, Calcium Signaling
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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